Rythemecity and automatecity of heart
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1) The document discusses the rhythmicity and automaticity of the heart, which refers to the heart's ability to beat regularly and generate impulses without external stimuli. 2) It originates from within the heart itself (myogenic, not neurogenic) and several factors can influence the heart rate such as the autonomic nervous system, temperature, drugs, blood gases, and inorganic ions. 3) The sinoatrial node acts as the pacemaker for the heart and has membrane properties that allow it to spontaneously depolarize, initiating the heartbeat via an action potential involving sodium, calcium, and potassium ion fluxes.
Rythemecity and automatecity of heart
- 1. PresentationTOPIC RYTHEMECITYANDAUTOMATECITYOFHEART Presented By: 1) Romeen Yasmeen 2) Safi Ullah 3) Rooh Niaz Submitted To : Ms. Naila Gul
- 4. DEF. • Rhythmicity is the ability of heart to beat regularly • Automaticity is the ability of heart to generate impulses without external stimuli • Autorhythmicity is the ability of cardiac ms to generate impulses without external stimuli at regular rate
- 5. •Origin • Myogenic not neurogenic. • The nerves control the rate but do not initiate the beat Evidences: a) Local anesthetics e.g. cocaine block the nerve but not stop the heart
- 6. B) Transplanted heart (No nerve supply) continues to beat. C) heart of human fetus start to beat before development of nerves
- 7. • Nature: • Most cardiac fibers have the ability of self excitation especially nodal and conducting fibers • SAN has the greatest rhythm, so it is called "pace maker of the heart
- 8. MECHANISM OF AUTORHYTHMICITY OF SAN: •RMP of SAN is low about -55mv to -60 mv. •This is due to natural leakiness to Na ions Action Potential (AP): 1. Prepotential or pacemaker potential (phase 4) 2. Upstroke (phase 0) 3. Repolarization (phase 3)
- 9. It is a gradual rise of membrane potential from the resting level of -55 mv to the firing level or the threshold voltage of -40 mv Mechanism: 1. Na influx through funny (slow) Na channels 2. Ca influx through T (=transient) -type Ca channel 3. Decreased K+ efflux It occurs during diastole, so it is also called the diastolic depolarization (DD)
- 10. Importance of Pacemaker potential: 1. It is the cause of Rhythmicity. 2. The rate of slope of the prepotential determines the heart rate. The more rapid is the slope, the more will be the heart rate.
- 11. 2. UPSTROKE (PHASE 0): Mechanism: • Inward Ca++ current through L (long lasting ) Ca++ channels •From membrane potential (– 40 m.v) to (+ 10 m.v)
- 12. 3. Repolarization (phase 3): Mechanism: • increase K+ efflux •From membrane potential (+10 m.v) to (-60 m.v)
- 14. -60 -40 - 20 - 10 0 +10 Phase 0 Phase 3 Na+ ca++ mv R.M.P Na+ m Na+ Na+ Na+Na+ Na+ h K+ ca++ K+ K+K+ ca++ca++ K+K+K+ Depolarization Phase 4 (only in pacemaker cells Repolarization ca++ ca++ca++ ca++ ca++ca++ca++
- 16. FACTORS AFFECTING RHYTHMICITY • CHRONOTROPISM MEANS AN INFLUENCE ON THE HEART RATE • +VE CHRONOTROPIC → ↑ HEART RATE • -VE CHRONOTROPIC → ↓ HEART RATE Dra abdelaziz Hussein, Mansoura Faculty of Medicine Factor s Nervous Factors sympat hetic Parasy mpath etic Physical Warming and cooling Chemical Drug s Gases Ions Toxin s
- 18. AUTONOMIC N. SYSTEM SYMPATHETIC STIMULATION: • HAS A +VE CHRONOTROPIC EFFECT Figure 14-17: Modulation of heart rate by the nervous system •Release noradrenalin → increases fiber membrane permeability to Na+ & Ca++→ rapid slope of Prepotential → threshold is reached rapidly → increase Rhythmicity
- 19. AUTONOMIC N. SYSTEM PARASYMPATHETIC STIMULATION: • HAS A -VE CHRONOTROPIC EFFECT Figure 14-17: Modulation of heart rate by the nervous system •Acetylcholine released at the vagal endings →increase the permeability of fiber membrane to K+ → rapid K+ efflux → hyperpolarization→ decrease Rhythmicity
- 20. PHYSICAL FACTORS WARMING: • MODERATE WARMING : INCREASES RHYTHMICITY DUE TO; a)↓permeability of the membrane to K+ ions during the pacemaker potential, i.e. rapid slope of prepotential b)↑speed of ionic fluxes across the membrane during the action potential •Excessive warming (45 ) denatures the intracellular proteins and produces cardiac damage •Moderate cooling decreases Rhythmicity •Excessive cooling stop Rhythmicity
- 21. CHEMICAL FACTORS 1. DRUGS AND HORMONES:•Catecholamines have +ve chronotropic effect. •Cholinergic drugs (as methacholine) have –ve chronotropic effect •Thyroxine has a +ve chronotropic effect as it stimulates the metabolism of the SAN. •Digitalis depresses nodal tissue. It increases K+ efflux → hyperpolarization
- 22. CHEMICAL FACTORS 2. BLOOD GASES: •O2 lack (hypoxia): •Mild hypoxia increases rhythmicity •Severe hypoxia decreases and stop rhythmicity •Hypercapnia: has a -ve chronotropic effect through acidemia •H ion concentration : •Acidosis decreases rhythmicity •Alkalosis increases rhythmicity •Severe acidosis and alkalosis decreases rhythmicity .
- 23. CHEMICAL FACTORS 3. INORGANIC IONS : •K ions : • mild hyperkalemia have -ve chronotropic effect. (because excess K in ECF decreases K efflux during repolarization) •Mild hypokalemia has opposite effect •Ca ions: • Mild increase of Ca++ (hypercalcemia) decreases rhythmicity by activating K+ channels → hyperpolarization → so longer time is needed to reach threshold potential. •Mild hypocalemia has the opposite
- 24. CHEMICAL FACTORS 3. INORGANIC IONS : •K ions : • mild hyperkalemia have -ve chronotropic effect. (because excess K in ECF decreases K efflux during repolarization) •Mild hypokalemia has opposite effect •Ca ions: • Mild increase of Ca++ (hypercalcemia) decreases rhythmicity by activating K+ channels → hyperpolarization → so longer time is needed to reach threshold potential. •Mild hypocalemia has the opposite
- 25. TOXINS •Typhoid or diphtheria toxins have a –ve chronotropic effect, due to direct inhibitory action on nodal tissues